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  1. Article ; Online: Repressor Element-1 Binding Transcription Factor (REST) as a Possible Epigenetic Regulator of Neurodegeneration and MicroRNA-Based Therapeutic Strategies.

    Nassar, Ajmal / Satarker, Sairaj / Gurram, Prasada Chowdari / Upadhya, Dinesh / Fayaz, S M / Nampoothiri, Madhavan

    Molecular neurobiology

    2023  Volume 60, Issue 10, Page(s) 5557–5577

    Abstract: Neurodegenerative disorders (NDD) have grabbed significant scientific consideration due to their fast increase in prevalence worldwide. The specific pathophysiology of the disease and the amazing changes in the brain that take place as it advances are ... ...

    Abstract Neurodegenerative disorders (NDD) have grabbed significant scientific consideration due to their fast increase in prevalence worldwide. The specific pathophysiology of the disease and the amazing changes in the brain that take place as it advances are still the top issues of contemporary research. Transcription factors play a decisive role in integrating various signal transduction pathways to ensure homeostasis. Disruptions in the regulation of transcription can result in various pathologies, including NDD. Numerous microRNAs and epigenetic transcription factors have emerged as candidates for determining the precise etiology of NDD. Consequently, understanding by what means transcription factors are regulated and how the deregulation of transcription factors contributes to neurological dysfunction is important to the therapeutic targeting of pathways that they modulate. RE1-silencing transcription factor (REST) also named neuron-restrictive silencer factor (NRSF) has been studied in the pathophysiology of NDD. REST was realized to be a part of a neuroprotective element with the ability to be tuned and influenced by numerous microRNAs, such as microRNAs 124, 132, and 9 implicated in NDD. This article looks at the role of REST and the influence of various microRNAs in controlling REST function in the progression of Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD) disease. Furthermore, to therapeutically exploit the possibility of targeting various microRNAs, we bring forth an overview of drug-delivery systems to modulate the microRNAs regulating REST in NDD.
    MeSH term(s) Humans ; Transcription Factors/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; MicroRNAs/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/therapy ; Epigenesis, Genetic
    Chemical Substances Transcription Factors ; RE1-silencing transcription factor ; Repressor Proteins ; MicroRNAs
    Language English
    Publishing date 2023-06-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03437-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2411: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Astrocytic transcription factors REST, YY1, and putative microRNAs in Parkinson's disease and advanced therapeutic strategies.

    Nassar, Ajmal / Kodi, Triveni / Satarker, Sairaj / Gurram, Prasada Chowdari / Fayaz, S M / Nampoothiri, Madhavan

    Gene

    2023  Volume 892, Page(s) 147898

    Abstract: Transcription factors (TF) and microRNAs are regulatory factors in astrocytes and are linked to several Parkinson's disease (PD) progression causes, such as disruption of glutamine transporters in astrocytes and concomitant disrupted glutamine uptake and ...

    Abstract Transcription factors (TF) and microRNAs are regulatory factors in astrocytes and are linked to several Parkinson's disease (PD) progression causes, such as disruption of glutamine transporters in astrocytes and concomitant disrupted glutamine uptake and inflammation. REST, a crucial TF, has been documented as an epigenetic repressor that limits the expression of neuronal genes in non-neural cells. REST activity is significantly linked to its corepressors in astrocytes, specifically histone deacetylases (HDACs), CoREST, and MECP2. Another REST-regulating TF, YY1, has been studied in astrocytes, and its interaction with REST has been investigated. In this review, the molecular processes that support the astrocytic control of REST and YY1 in terms of the regulation of glutamate transporter EAAT2 were addressed in a more detailed and comprehensive manner. Both TFs' function in astrocytes and how astrocyte abnormalities cause PD is still a mystery. Moreover, microRNAs (short non-coding RNAs) are key regulators that have been correlated to the expression and regulation of numerous genes linked to PD. The identification of numerous miRs that are engaged in astrocyte dysfunction that triggers PD has been shown. The term "Gut-brain axis" refers to the two systems' mutual communication. Gut microbial dysbiosis, which mediates an imbalance of the gut-brain axis, might contribute to neurodegenerative illnesses through altered astrocytic regulation. New treatment approaches to modify the gut-brain axis and prevent astrocytic repercussions have also been investigated in this review.
    MeSH term(s) Humans ; Transcription Factors/metabolism ; Astrocytes/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Glutamine/metabolism ; YY1 Transcription Factor/genetics ; YY1 Transcription Factor/metabolism
    Chemical Substances Transcription Factors ; MicroRNAs ; Glutamine (0RH81L854J) ; YY1 protein, human ; YY1 Transcription Factor
    Language English
    Publishing date 2023-10-11
    Publishing country Netherlands
    Document type Review ; Journal Article
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2023.147898
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1357: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Astrocytic MicroRNAs and Transcription Factors in Alzheimer's Disease and Therapeutic Interventions.

    Nassar, Ajmal / Kodi, Triveni / Satarker, Sairaj / Chowdari Gurram, Prasada / Upadhya, Dinesh / Sm, Fayaz / Mudgal, Jayesh / Nampoothiri, Madhavan

    Cells

    2022  Volume 11, Issue 24

    Abstract: Astrocytes are important for maintaining cholesterol metabolism, glutamate uptake, and neurotransmission. Indeed, inflammatory processes and neurodegeneration contribute to the altered morphology, gene expression, and function of astrocytes. Astrocytes, ... ...

    Abstract Astrocytes are important for maintaining cholesterol metabolism, glutamate uptake, and neurotransmission. Indeed, inflammatory processes and neurodegeneration contribute to the altered morphology, gene expression, and function of astrocytes. Astrocytes, in collaboration with numerous microRNAs, regulate brain cholesterol levels as well as glutamatergic and inflammatory signaling, all of which contribute to general brain homeostasis. Neural electrical activity, synaptic plasticity processes, learning, and memory are dependent on the astrocyte-neuron crosstalk. Here, we review the involvement of astrocytic microRNAs that potentially regulate cholesterol metabolism, glutamate uptake, and inflammation in Alzheimer's disease (AD). The interaction between astrocytic microRNAs and long non-coding RNA and transcription factors specific to astrocytes also contributes to the pathogenesis of AD. Thus, astrocytic microRNAs arise as a promising target, as AD conditions are a worldwide public health problem. This review examines novel therapeutic strategies to target astrocyte dysfunction in AD, such as lipid nanodiscs, engineered G protein-coupled receptors, extracellular vesicles, and nanoparticles.
    Language English
    Publishing date 2022-12-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11244111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Evaluating the Role of N-Acetyl-L-Tryptophan in the Aβ 1-42-Induced Neuroinflammation and Cognitive Decline in Alzheimer's Disease.

    Satarker, Sairaj / Gurram, Prasada Chowdari / Nassar, Ajmal / Manandhar, Suman / Vibhavari, Rja / Yarlagadda, Dani Lakshman / Mudgal, Jayesh / Lewis, Shaila / Arora, Devinder / Nampoothiri, Madhavan

    Molecular neurobiology

    2023  

    Abstract: Alzheimer's disease (AD), a neurodegenerative condition previously known to affect the older population, is also now seen in younger individuals. AD is often associated with cognitive decline and neuroinflammation elevation primarily due to amyloid β (Aβ) ...

    Abstract Alzheimer's disease (AD), a neurodegenerative condition previously known to affect the older population, is also now seen in younger individuals. AD is often associated with cognitive decline and neuroinflammation elevation primarily due to amyloid β (Aβ) accumulation. Multiple pathological complications in AD call for therapies with a wide range of neuroprotection. Our study aims to evaluate the effect of N-acetyl-L-tryptophan (NAT) in ameliorating the cognitive decline and neuroinflammation induced by Aβ 1-42 oligomers and to determine the therapeutic concentration of NAT in the brain. We administered Aβ 1-42 oligomers in rats via intracerebroventricular (i.c.v.) injection to induce AD-like conditions. The NAT-treated animals lowered the cognitive decline in the Morris water maze characterized by shorter escape latency and increased path efficiency and platform entries. Interestingly, the hippocampus and frontal cortex showed downregulation of tumor necrosis factor, interleukin-6, and substance P levels. NAT treatment also reduced acetylcholinesterase activity and total and phosphorylated nuclear factor kappa B and Tau levels. Lastly, we observed upregulation of cAMP response element-binding protein 1 (CREB1) signaling. Surprisingly, our HPLC method was not sensitive enough to detect the therapeutic levels of NAT in the brain, possibly due to NAT concentrations being below the lowest limit of quantification of our validated method. To summarize, the administration of NAT significantly lowered cognitive decline, neuroinflammatory pathways, and Tau protein and triggered the upregulation of CREB1 signaling, suggesting its neuroprotective role in AD-like conditions.
    Language English
    Publishing date 2023-12-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03844-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2411: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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